This research plan will study the mechanism of pressure induced interruption of optic nerve axonal transport in animal eyes with acute experimental pressure elevation. More specifically, the effects of pharmacologic reduction in ocular blood flow upon this transport interruption will be investigated. In addition, this effort will test the hypothesis that pressure induced deformation of structurally weaker regions of the nerve head lamina cribrosa causes this transport interruption. Finally, analysis of preferential involvement of optic nerve axons by this phenomenon will be made to test the hypothesis that specific axon types are most susceptible to this damage.